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Suppressor of cytokine signalling (SOCS) 1 and 3 enhance cell adhesion and inhibit migration towards the chemokine eotaxin/CCL11
Author(s) -
Stevenson Nigel J.,
McFarlane Cheryl,
Ong Seow Theng,
Nahlik Krystyna,
Kelvin Alyson,
Addley Mark R.,
Long Aideen,
Greaves David R.,
O'Farrelly Cliona,
Johnston James A.
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.10.007
Subject(s) - rhoa , microbiology and biotechnology , suppressor of cytokine signaling 1 , chemokine , focal adhesion , cell adhesion , suppressor of cytokine signalling , tyrosine phosphorylation , signal transduction , chemokine receptor , cell migration , chemistry , socs3 , biology , adhesion , immunology , inflammation , stat3 , cell , suppressor , biochemistry , organic chemistry , gene
Suppressors of cytokine signalling (SOCS) proteins regulate signal transduction, but their role in responses to chemokines remains poorly understood. We report that cells expressing SOCS1 and 3 exhibit enhanced adhesion and reduced migration towards the chemokine CCL11. Focal adhesion kinase (FAK) and the GTPase RhoA, control cell adhesion and migration and we show the presence of SOCS1 or 3 regulates expression and tyrosine phosphorylation of FAK, while also enhancing activation of RhoA. Our novel findings suggest that SOCS1 and 3 may control chemotaxis and adhesion by significantly enhancing both FAK and RhoA activity, thus localizing immune cells to the site of allergic inflammation.